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Göteborgs universitet
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  4. Martin Lagging

Martin Lagging

±Ê°ù´Ç´Ú±ð²õ²õ´Ç°ù/ö±¹±ð°ù±ôä°ì²¹°ù±ð

Avd för infektionssjukdomar
Telefon
031-342 47 31
0705-68 37 59
E-post
martin.lagging@gu.se
Fax
031-41 12 56
µþ±ð²õö°ì²õ²¹»å°ù±ð²õ²õ
Guldhedsgatan 10A
41346 Göteborg
Rumsnummer
VÃ¥ning 5
Postadress
Guldhedsgatan 10A
41346 Göteborg

Om Martin Lagging

Role of Genetic Variations of Innate Immunity in Microbial Infections

Research Focus:

Our group has focused on translational studies and interventional/therapeutic trials on hepatitis C virus (HCV) with the goal of improving outcome as well as minimizing the risk of adverse events. In particular, we evaluated the impact of host factors such as interferon-gamma inducible protein 10 (IP-10; also known as CXCL10) as well human genetic variants, e.g. in the gene coding for interferon-lambda 4 (IFNL4; previously known as IL28B), on liver histopathology, response to therapy, and outcome for HCV treatment.

More recently, we have evaluated the impact of genetic variations in the inosine triphosphate pyrophosphatase (ITPase) gene on HCV infection, and reported a novel ribavirin-like reduced risk of relapse among patients having reduced ITPase activity. The evolutionary conserved ITPase is a cytosolic enzyme that recycles purines by the pyrophosphohydrolysis of ITP to inosine monophosphate (IMP), and thus protects against accumulation of non-canonical nucleotides such as ITP and xanthosine triphosphate (XTP) as well as their deoxy forms (dITP and dXTP), which otherwise incorrectly may be incorporated into RNA and DNA producing genetic instability, anomalous proteins, and altered ATP-dependent signaling.

In the near future, we plan to expand our evaluation of ITPase to include other microbial infections, as we hypothesize that inhibition of ITPase may point to novel antiviral and antibacterial strategies.